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Generally speaking, early tracheostomies are recommended for patients who have anatomical anomalies that make emergent intubation difficult or impossible. These include many head
and neck surgery patients and patients with head and neck infections causing trismus or airway
obstruction.
17. What is the purpose of downsizing a tracheostomy? How do you downsize a
tracheostomy?
The indications for downsizing a tracheostomy include improving patient comfort, reducing pressure
on the tracheal mucosa, and facilitating the passage of air around the tracheostomy tube for speech.
Typically, as a prerequisite, the patient should have had the tracheostomy in place for at least 7 to
10 days to ensure a proper track has formed, thus making tube exchange less risky. The patient must
be hemodynamically stable, and off mechanical ventilation.
It is prudent to have the patient in a monitored environment with pulse oximetry during the
decannulation process. The patient should be preoxygenated and the tracheostomy tube and oropharynx suctioned to remove any secretions that may become dislodged when the cuff is deflated. The
patient should be placed in a supine position with the neck extended. Any sutures or ties securing the
tracheostomy tube are removed, the cuff, if present, is deflated, the old tube is removed at the peak
of inspiration, and the new, smaller tracheostomy tube is inserted with the obturator in place. The
new tracheostomy tube is secured, and the patient is monitored to ensure no respiratory distress is
present. This procedure may also be performed over a tube exchanger to ensure that the tube is not
placed in a false passage.
18. What are the most common life-threatening postoperative complications of a
tracheostomy?
Hemorrhage, tube dislodgment, and tube obstruction.
19. What are the possible causes of postoperative bleeding in tracheostomy
patients?
A small amount of bleeding from the tissues surrounding a recent tracheostomy is common
and can usually be controlled with local measures such as pressure dressings around the
tracheostomy tube. Continued bleeding that does not resolve may be an indication for surgical
exploration. Tracheo-innominate fistula is a rare complication that may result in catastrophic
hemorrhage.
20. What do you do if a tracheostomy tube becomes dislodged?
Management of accidental decannulation depends on an initial, rapid evaluation of the patient’s oxy-
genation and ventilation status. If the patient is not in apparent respiratory distress, then one should
carefully attempt reinserting a well-lubricated tube with the obturator in place; consideration should
be given to inserting a smaller tube if available.
In situations when the tracheostomy was placed recently and the tract is not yet fully formed,
rapid replacement of the tube is paramount as the tract may collapse, making simple replacement of
the tube impossible. If stay sutures are present, apply traction to bring the trachea anteriorly, facilitating insertion.
If the patient is in respiratory distress, then one should administer supplemental oxygen and
consider oral bag mask ventilation and orotracheal intubation.
Ultimately, the most important factor is preventing dislodgment in the first place. This involves
ensuring that an appropriately sized tube is selected, there is no excessive coughing or agitation, the
tube is properly secured, and the patient is appropriately monitored.
21. What do you do if a tracheostomy tube is obstructed?
A possible cause of respiratory distress in a tracheostomy patient is tube obstruction. One must
initially inspect the inner cannula; if any mucus plugging is noted, it can be readily replaced with a
clean one. Continued respiratory distress may indicate that the tube has been displaced into a false
passage or that there is an obstruction in the distal tube or trachea itself. A bedside maneuver that
can be performed to further elucidate the nature of the distress is passing a soft suction catheter. If it
passes easily and secretions are readily suctioned, that suggests that the tube was partially obstructed
by secretions. If one is unable to pass the soft suction catheter more than a few centimeters, the
tube may be lodged in a false passage or the tube itself may be clogged. In patients with immature
stomas, the best course of action is to then secure the airway via an orotracheal tube, thus providing
an opportunity to revise the tracheostomy.
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22. How do you identify and manage a tracheo-innominate (TI) fistula?
A TI fistula is one of the most life-threatening tracheostomy complications. Associated risk factors
include overinflated cuff, high-pressure cuff, excessive movement of the tracheostomy, and caudal
tracheostomy placement. The pathophysiology involves pressure of the cuff or tube on the tracheal
mucosa, eventually eroding through the trachea and into the innominate (brachiocephalic) artery,
which typically is located at the ninth tracheal ring. The complication most commonly occurs at the
third to fourth postoperative week, and mortality approaches 100%.
This complication is avoided by preventing prolonged hyperextension of the patient’s neck, using
lightweight tubing to avoid traction of the tracheostomy tube, and deflating the cuff when mechanical
ventilation is no longer necessary.
Early diagnosis is said to be the key to successful management. Many patients have sentinel
hemorrhages that precede the devastating hemorrhage. These should be evaluated appropriately. A
ridged bronchoscopy may be performed in a setting where potential intervention is possible. If inconclusive, angiography should be performed to further elucidate the vascular anatomy.
In the event of an acute hemorrhage, an attempt must be made to control the hemorrhage at bedside. The cuff is overinflated, and the tube withdrawn with pressure directed at the anterior tracheal wall,
in an attempt to occlude the innominate artery. If this fails, the patient should be orally intubated, the tracheostomy tube should be removed, and a finger can be used to bluntly dissect through the pretracheal
fascia, attempting to occlude the artery against the anterior chest wall. If successful, the maneuvers can
be used to help stabilize the patient during transport to the operating room for definitive management.
23. What are the advantages of a percutaneous tracheostomy (PCT)?
The advantages of percutaneous techniques are that they use smaller incisions, cause potentially less
tissue trauma, are potentially less invasive, are more readily performed at bedside in a critical care
setting, and, according to some studies, have lower complication rates. There are multiple techniques
described in the literature for performing a PCT, as well as several commercially available kits.
24. What is the surgical technique for a percutaneous tracheostomy?
The patient is positioned, prepped, and draped in the same manner as for a standard tracheostomy,
with the neck extended. Anatomical landmarks are identified, including the cricothyroid membrane
and the sternal notch; ideally the entrance point into the trachea is to be at the second and third rings.
A bronchoscope is then passed into the airway, and the tracheal anatomy is visualized. The bronchoscope is then used to monitor the placement of the introducer needle as well as subsequent dilation
and eventual insertion of the tracheostomy tube.
Localanesthesiawithepinephrineisadministeredintotheplannedsurgicalsite,anda1-cm
incision is made in the midline, through the skin and subcutaneous tissue. The introducer needle
is then inserted at a 45-degree angle to the skin until air is aspirated. Care is taken to not advance
the needle through the posterior wall of the trachea, and the needle introduction is simultaneously
observed through the bronchoscope to ensure correct positioning.
In what is referred to as the Seldinger technique, a guide wire is then passed through the
introducer needle into the trachea. The needle is then removed, and a lubricated dilator is passed
over the wire. Depending on the set used, there are variations in the dilator sequence and specific
dilating instruments. The basic concept, however, remains unchanged. Once dilated to the appropriate
diameter, the tracheostomy tube is inserted. Once in place, the ET tube is withdrawn, end-tidal CO2 is
confirmed, peak pressures and tidal volumes are confirmed, and the tracheostomy tube is secured.
It is important to note that when performing a percutaneous tracheostomy, one must always be
prepared to convert to a standard open tracheostomy in the event that complications occur.
25. What is the purpose of the inner cannula, and how should it be cared for?
Inner cannulas should be regularly examined and cleaned both for hygiene as well as to prevent
mucus plugging. Many clinicians recommend that they be checked several times daily. Mucus plugging is one possible cause of an airway emergency in a tracheostomy-dependent patient that can be
easily mitigated by regular inner cannula changes.
26. Do tracheostomy patients require speech and swallow evaluations prior to feeding? Does the inflated cuff prevent aspiration?
Currently, there is no evidence that placement of a tracheostomy results in increased rates of
dysphagia and aspiration. Instead it appears that aspiration postoperatively is more dependent on the
patient’s preoperative status, prolonged mechanical ventilation, and associated comorbid conditions
that may affect the swallowing mechanisms. As such, patients who do not have associated physical or
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cognitive deficits that might result in aspiration do not require a speech and swallow evaluation prior
to resuming oral intake.
The inflated cuff does not provide much protection against aspiration, as secretions will eventu-
ally leak around the cuff unless frequently suctioned.
27. What is the process of decannulation?
Decannulation is the final step in weaning a patient from a tracheostomy and may occur when a
patient no longer requires mechanical ventilation or airway protection. Typically a patient’s tracheostomy tube is gradually downsized until translaryngeal air is able to pass around the tube to the point
thatitispossibleto“cap”thetubewithoutanyevidenceofrespiratorydistress.Insituationswhenit
is not expected that the patient will undergo further operations, it acceptable to remove the tracheos-
tomytubeifthepatienthasbeenabletotoleratea“capped”tubefor48hours.Immediatelyfollowing
removal of the tube, a dressing is placed on the stoma. One option is to use petroleum gauze secured
with silk tape. The patient is instructed to apply pressure to the dressing when speaking or coughing,
thus preventing the dressing from becoming dislodged. The dressing should be changed daily until the
stoma closes over the next several days to weeks.
BiBliography
Abubaker AO, Benson KJ: Tracheostomy and cricothyrotomy. In Oral and maxillofacial surgery secrets,ed2,StLouis,2007,
Mosby Elsevier.
Allan JS, Wright CD: Tracheoinnominate fistula: diagnosis and management, Chest Surg Clin N Am 13:331, 2003.
Bradley PJ: Management of airway and tracheostomy. In Hibbert J, editor: Otolaryngology: laryngology and head and neck
surgery, ed 6, Bath, England, 1997, Butterworth–Heinernann.
Braun RF, Cutilli BJ: Cricothyrotomy. In Braun RF, Cutilli BJ, editors: Manual of emergency medical treatment for the dental
team, Baltimore, 1999, Williams & Wilkins.
Demas PN, Sotereanos GC: The use of tracheotomy in oral and maxillofacial surgery, J Oral Maxillofac Surg 46:483–486, 1988.
Engels PT, Bagshaw SM, Meier M, Brindley PG: Tracheostomy: from insertion to decannulation, Can J Surg 52:427, 2009.
Epstein SK:Latecomplicationsoftracheostomy,Respir Care 50:542, 2005.
Feinberg SE,PetersonLJ: Use of cricothyrotomy in oral and maxillofacial surgery, J Oral Maxillofac Surg 45:873–878, 1987.
Groves DS, Durbin Jr. CG: Tracheostomy in the critically ill: indications, timing and techniques, Curr Opin Crit Care 13:90, 2007.
Jones JW, Reynolds M, Hewitt RL, Drapanas T: Tracheo-innominate artery erosion: successful surgical management of a
devastating complication, Ann Surg 184:194, 1976.
Koch T, Hecker B, Hecker A, et al.: Early tracheostomy decreases ventilation time but has no impact on mortality of inten-
sive care patients: a randomized study, Langenbecks Arch Surg 397:1001, 2012.
LederSB, Ross DA: Confirmation of no causal relationship between tracheotomy and aspiration status: a direct replication
study, Dysphagia 25:35, 2010.
LewisRJ: Tracheostomy. Indications, timing, and complications, Clinic Chest Med 13:137–149, 1992.
LoreJM:Emergencyprocedures.InLoreJM, Medina JE, editors: An atlas of head and neck surgery, ed 4, Philadelphia,
2005, Saunders.
Montgomery WW: Surgery of the upper respiratory system,ed2,Philadelphia,1989,Lea&Febiger.
MorrisLL, Whitmer A, McIntosh E: Tracheostomy care and complications in the intensive care unit, Crit Care Nurse 33:18, 2013.
Parsons DS, Smith WC: Difficult tracheostomy decannulation. In Gates GA, editor: Current therapy in otolaryngology head
and neck surgery,ed6,StLouis,1998,Mosby.
Patel RG: Percutaneous transtracheal jet ventilation: a safe, quick, and temporary way to provide oxygenation and ventila-
tion when conventional methods are unsuccessful, Chest 116:1689, 1999.
Paul A, Marelli D, Chiu RC, Vestweber KH, Mulder DS: Percutaneous endoscopic tracheostomy, Ann Thorac Surg 47:314, 1989.
Plummer AL, Gracey DR: Consensus conference on artificial airways in patients receiving mechanical ventilation, Chest
96:178, 1989.
Stothert Jr JC, Stout MJ,LewisLM, Keltner Jr RM: High pressure percutaneous transtracheal ventilation: the use of large
gauge intravenous-type catheters in the totally obstructed airway, Am J Emerg Med 8:184, 1990.
Terk AR,LederSB, Burrell MI: Hyoid bone and laryngeal movement dependent upon presence of a tracheotomy tube,
Dysphagia 22:89, 2007.
Weissler MC: Tracheostomy and intubation. In Bailey BJ, editor: Head and neck surgery–otolaryngology, Philadelphia, 1993,
J.B.Lippincott.
White AC, Kher S, O’Connor HH: When to change a tracheostomy tube, Respir Care 55:1069, 2010.
IV
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ManageMent
Considerations for the
MediCally-CoMproMised
patients
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O2content = [1.39 mL O2/g of hemoglobin × hemoglobin (g/dL) × % saturation]
+
CARDIOVASCULAR DISEASES:
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ISCHEMIC HEART DISEASE,
MYOCARDIAL INFARCTION, AND
VALVULAR HEART DISEASE
David W. Lui, A. Omar Abubaker
1. What are the known risk factors for the development of ischemic heart disease
(IHD)?
Age, male gender, positive family history, hypertension, smoking, hypercholesterolemia, and diabetes
mellitus. Sedentary lifestyle and obesity are often associated factors.
2. What are the determinants of myocardial oxygen supply and demand?
Oxygen (O2) supply to the myocardium is determined by oxygen content and coronary blood flow.
Oxygen content can be calculated by the following equation:
[0.003×PaO2]
Coronary blood flow occurs mainly during diastole, especially to the ventricular endocardium.
Coronary perfusion pressure is determined by the difference between diastolic blood pressure and
left ventricular end-diastolic pressure (LVEDP). Anemia, hypoxemia, tachycardia, diastolic hypotension,
hypocapnia (coronary vasoconstriction), coronary occlusion (IHD), vasospasm, increased LVEDP, and
hypertrophied myocardium all may adversely affect myocardial O2 supply.
Myocardial O2 demand is determined by heart rate, contractility, and wall tension.
Increases in heart rate increase myocardial work and decrease the relative time spent in
diastole (decreased supply). Contractility increases in response to sympathetic stimulation,
which increases O2 demand. Wall tension is the product of intraventricular pressure and radius.
Increased ventricular volume (preload) and increased blood pressure (BP) (afterload) both
increase wall tension and O2 demand.
3. What is the pathophysiology of myocardial ischemia?
Ischemia occurs when coronary blood flow is inadequate to meet the needs of the myocardium.
Atherosclerotic lesions that occlude 50% to 75% of the vessel lumen are considered hemodynamically
significant. Non-stenotic causes of ischemia include aortic valve disease, left ventricular hypertrophy,
ostial occlusion, coronary embolism, coronary arteritis, and vasospasm.
The right coronary artery system is dominant in 80% to 90% of people and supplies the sinoatrial node, atrioventricular node, and right ventricle. Right-sided coronary artery disease often manifests as heart block and dysrhythmias. The left main coronary artery gives rise to the circumflex artery
and left anterior descending artery, which supply the majority of the interventricular septum and left
ventricular wall. Significant stenosis of the left main coronary artery (left main disease) or the proximal
circumflex and left anterior descending arteries (left main equivalent) may cause severely depressed
myocardial function during ischemia.
4. What is the pathogenesis of a perioperative myocardial infarction?
A myocardial infarction (MI) is usually caused by platelet aggregation, vasoconstriction, and thrombus
formation at the site of an atheromatous plaque in a coronary artery. Sudden increases in myocardial
O2 demand (tachycardia, hypertension) or decreases in O2 supply (hypotension, hypoxemia, or anemia)
can precipitate MI in patients with IHD. Complications of MI include dysrhythmias, hypotension,
congestive heart failure (CHF), acute mitral regurgitation, pericarditis, ventricular thrombus formation,
ventricular rupture, and death.
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5. What clinical factors increase the risk of a perioperative MI following non-cardiac
surgery?
IHD (prior MI or angina) and CHF are historically the strongest predictors of an increased risk for
perioperative MI. Other risk factors include valvular heart disease (particularly aortic stenosis), arrhythmias caused by underlying heart disease, advanced age, type of surgical procedure, and poor general
medical status. Hypertension alone does not place a patient at increased risk for perioperative MI, but
these patients are at increased risk for IHD, CHF, and stroke.
6. How can cardiac function be evaluated on history and physical exam?
If a patient’s exercise capacity is excellent even in the presence of IHD, then chances are good that
the patient will be able to tolerate the stresses of surgery. Poor exercise tolerance in the absence of
pulmonary or other systemic disease indicates an inadequate cardiac reserve. All patients should be
questioned about their ability to perform daily activities, such as cleaning, yard work, shopping, and
golfing, for example. The ability to climb two to three flights of stairs without significant symptoms
(angina, dyspnea, syncope) is usually an indication of adequate cardiac reserve. Signs and symptoms
of CHF including dyspnea, orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, jugular
venous distention, a third heart sound, rales, and hepatomegaly must be recognized preoperatively.
7. What is the significance of a history of angina pectoris?
Angina is a symptom of myocardial ischemia, and nearly all patients with angina have coronary artery
disease. Stable angina is defined as no change in the onset, severity, and duration of chest pain for
at least 60 days. Syncope, shortness of breath, or dizziness that accompanies angina may indicate
severe myocardial dysfunction resulting from ischemia. Patients with unstable angina are at high
risk for developing an MI and should be referred for medical evaluation immediately. Patients with
diabetes mellitus and hypertension have a much higher incidence of silent ischemia. Perioperatively,
most ischemic episodes are silent (as determined by ambulatory and postoperative electrocardiogram
[ECG]) but probably significant in the final outcome of surgery.
8. Should all cardiac medications be continued throughout the perioperative period?
Patients with a history of IHD are usually taking medications intended to decrease myocardial oxygen
demand by decreasing the heart rate, preload, or contractile state (beta blockers, calcium channel
antagonists, nitrates) and to increase the oxygen supply by causing coronary vasodilation (nitrates).
These drugs are generally continued throughout the perioperative period. Abrupt withdrawal of beta
blockers can cause rebound increases in heart rate and BP. Calcium channel blockers can exaggerate
the myocardial depressant effects of inhaled anesthetics but should be continued perioperatively.
9. What ECG findings support the diagnosis of IHD?
The resting 12-lead ECG remains a low-cost, effective screening tool in the detection of IHD. It should
be evaluated for the presence of ST-segment depression or elevation, T-wave inversion, old MI as
demonstrated by Q waves, disturbances in conduction and rhythm, and left ventricular hypertrophy.
Ischemic changes in leads II, III, and aVF suggest right coronary artery disease, leads I and aVL monitor circumflex artery distribution, and leads V3-V5 look at the distribution of the left anterior descending artery. Poor progression of anterior forces suggests significant left ventricular dysfunction, possibly
related to IHD.
10. What tests performed by medical consultants can help further evaluate patients
with known or suspected IHD?
Exercise ECG is a noninvasive test that attempts to produce ischemic changes on ECG (ST depres-
sion = 1 mm from baseline) or symptoms by having the patient exercise to maximum capacity. Information obtained relates to the thresholds of heart rate and BP that can be tolerated. Maximal heart
rates and BP response, as well as symptoms, guide interpretation of results.
Exercise thallium scintigraphy increases the sensitivity and specificity of the exercise ECG. The
isotope thallium is almost completely taken up from the coronary circulation by the myocardium
and can then be visualized radiographically. Poorly perfused areas that later refill with contrast
delineate areas of myocardium at risk for ischemia. Fixed perfusion defects indicate infarcted
myocardium.
Dipyridamole thallium imaging is useful in patients who are unable to exercise. This testing
is frequently required in patients with peripheral vascular disease who are at high risk for IHD and
limited by claudication. Dipyridamole is a potent coronary vasodilator that causes differential flow
between normal and diseased coronary arteries detectable by thallium imaging.
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Echocardiography can be used to evaluate left ventricular and valvular function and to measure
ejection fraction. Stress echocardiography (dobutamine echo) can be used to evaluate new or worsened regional wall motion abnormalities in the pharmacologically stressed heart. Areas of wall motion
abnormality are considered at risk for ischemia.
Coronary angiography is the gold standard for defining the coronary anatomy. Valvular and
ventricular function can be evaluated and measurements of hemodynamic indices taken. Because
angiography is invasive, it is reserved for patients who require further evaluation based on previous
tests or who have a high probability of severe coronary disease.
11. Based on the initial evaluation, which patients should be referred for further
testing?
Patients at risk for IHD but with good exercise tolerance may not require further work-up, especially
if they are undergoing procedures with a low to moderate risk of perioperative MI. Patients with
decreased exercise tolerance for unclear reasons or with unreliable histories should be evaluated with
dipyridamole thallium testing.
Patients with documented IHD (prior MI or chronic, stable angina) with good exercise tolerance
can sometimes proceed with low-risk surgery without further evaluation. Patients with known IHD and
poor exercise tolerance should be referred for dipyridamole thallium testing or coronary angiography
before all but the most minor surgical procedures.
12. Which surgical procedures carry the highest risk of perioperative MI?
In general, major abdominal, thoracic, and emergency surgeries carry the highest risk of periopera-
tive MI. The highest risk non-cardiac procedure is aortic aneurysm repair. These patients have a high
incidence of IHD, and cross-clamping of the aorta during surgery and postoperative complications can
place great stress on the heart.
13. How long should a patient with a recent MI wait before undergoing elective noncardiac surgery?
The risk of re-infarction during surgery after a prior MI has traditionally depended on the time inter-
val between the MI and the procedure. The highest risk of re-infarction is between 0 and 3 months
post-MI; lower risk is from 3 to 6 months; and a baseline risk level is reached after 6 months
(approximately 5% in most studies). A study using discharge summaries demonstrated that the
postoperative MI rate decreased substantially as the length of time from MI to operation increased
(0 to 30 days = 32.8%; 31 to 60 days = 18.7%; 61 to 90 days = 8.4%; and 91 to 180 days = 5.9%), as
did the 30-day mortality rate (0 to 30 days = 14.2%; 31 to 60 days = 11.5%; 61 to 90 days = 10.5%;
and 91 to 180 days = 9.9%).
14. What if surgery cannot safely be delayed for 6 months?
The patient’s functional status after rehabilitation from an MI is probably more important than the
absolute time interval. Patients with ongoing symptoms may be candidates for coronary revascularization before their non-cardiac procedure. Patients who quickly return to good functional status after
an MI can be considered for necessary non-cardiac surgery between 6 weeks and 3 months without
undue added risk, due to the advance of percutaneous coronary intervention. According to 2014
American College of Cardiology/American Heart Association perioperative guidelines, ≥ 60 days should
elapse after an MI before non-cardiac surgery in the absence of a coronary intervention.
15. How is premedication useful in the setting of IHD and surgery?
Patient anxiety can lead to catecholamine secretion and increased oxygen demand. In this regard, the
goal of premedication is to produce sedation and amnesia without causing deleterious myocardial
depression, hypotension, or hypoxemia. Morphine, scopolamine, and benzodiazepines, alone or in
combination, are popular choices to achieve these goals. All premedicated patients should receive
supplemental oxygen. Patients who use sublingual nitroglycerin should have access to their medication. Transdermal nitroglycerin can be applied in the perioperative period as well.
16. What are the hemodynamic goals of induction and maintenance of general
anesthesia in patients with IHD?
The anesthesiologist’s goal must be to maintain the balance between myocardial O2 supply and
demand throughout the perioperative period. During induction, wide swings in heart rate and BP
should be avoided. Ketamine should be avoided because of the resultant tachycardia and hypertension. Prolonged laryngoscopy should be avoided, and the anesthesiologist may wish to blunt the
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stimulation of laryngoscopy and intubation by the addition of opiates, beta blockers, or laryngotracheal
or intravenous lidocaine.
Maintenance drugs are chosen with knowledge of the patient’s ventricular function. In patients
with good left ventricular function, the cardiac depressant and vasodilatory effects of inhaled anesthetics may reduce myocardial O2 demand. A narcotic-based technique may be chosen to avoid undue
myocardial depression in patients with poor left ventricular function. Muscle relaxants with minimal
cardiovascular effects are usually preferred.
BP and heart rate should be maintained near baseline values. This can be accomplished by
blunting sympathetic stimulation with adequate analgesia and aggressively treating hypertension
(anesthetics, nitroglycerin, nitroprusside, beta blockers), hypotension (fluids, sympathomimetics,
inotropic drugs), and tachycardia (fluids, anesthetics, beta blockers).
17. What monitors are useful for detecting ischemia intraoperatively?
The V5 precordial lead is the most sensitive single ECG lead for detecting ischemia and should be
monitored routinely in patients at risk for IHD. Lead II can detect ischemia of the right coronary artery
distribution and is the most useful lead for monitoring P waves and cardiac rhythm.
Transesophageal echocardiography can provide continuous intraoperative monitoring of left
ventricular function. Detection of regional wall motion abnormalities with this technique is the most
sensitive for myocardial ischemia.
The pulmonary artery occlusion (wedge) pressure gives an indirect measurement of left ventricular volume and is a useful guide for optimizing intravascular fluid therapy. Sudden increases in the
wedge pressure may indicate acute left ventricular dysfunction resulting from ischemia. The routine
use of pulmonary artery catheters in patients with IHD has not been shown to improve outcome. However, close hemodynamic monitoring (including pulmonary artery catheter data) may be beneficial,
depending on the patient’s condition and the nature of the surgical procedure.
18. What is the basic pathophysiology of valvular heart disease?
Mitral and aortic stenosis cause pressure overload of the left ventricle, which produces hypertrophy
with a cardiac chamber of normal size. Mitral and aortic regurgitation causes volume overload, which
leads to hypertrophy with a dilated chamber. The net effect of left-sided valvular lesions is an impedance to forward flow of blood into the systemic circulation. Although right-sided valvular lesions occur,
left-sided lesions are more common and usually more hemodynamically significant. This chapter
deals only with left-sided lesions.
19. What are common findings of the history and physical exam in patients with valvular heart disease?
A history of rheumatic fever, intravenous drug abuse, or heart murmur should alert the examiner to the
possibility of valvular heart disease. Exercise tolerance is frequently decreased. Patients may exhibit
signs and symptoms of CHF, including dyspnea, orthopnea, fatigue, pulmonary rales, jugular venous
congestion, hepatic congestion, and dependent edema. Compensatory increases in sympathetic
nervous system tone manifest as resting tachycardia, anxiety, and diaphoresis. Angina may occur in
patients with a hypertrophied left ventricle, even in the absence of coronary artery disease. Atrial fibrillation frequently accompanies diseases of the mitral valve.
20. Which tests are useful in the evaluation of valvular heart disease?
The EGC should be examined for evidence of ischemia, arrhythmias, atrial enlargement, and ven-
tricular hypertrophy. The chest radiograph may show enlargement of cardiac chambers, suggest
pulmonary hypertension, or reveal pulmonary edema and pleural effusions. Cardiac catheterization
is the gold standard in the evaluation of such patients and determines pressures in various heart
chambers, as well as pressure gradients across valves. Cardiac angiography allows visualization of
the coronary arteries and heart chambers.
21. How is echocardiography helpful?
Doppler echocardiography characterizes ventricular function and valve function. It can be used to
measure the valve orifice area and transvalvular pressure gradients, which are measures of the severity
of valvular dysfunction. The function of prosthetic valves is also measured echocardiographically.
22. Which invasive monitors aid the anesthesiologist in the perioperative period?
An arterial catheter provides beat-to-beat BP measurement and continuous access to the bloodstream
for sampling. Pulmonary artery catheters enable the anesthetist to measure cardiac output and
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provide central access for the infusion of vasoactive drugs. The pulmonary capillary wedge pressure
is an index of left ventricular filling and is useful for guiding intravenous fluid therapy. Transesophageal
echocardiography can be used intraoperatively to evaluate left ventricular volume and function, to
detect ischemia (segmental wall motion abnormalities) and intracardiac air, and to examine valve
function before and after repair.
23. What is a pressure–volume loop?
A pressure–volume loop plots left ventricular pressure against volume through one complete cardiac
cycle. Each valvular lesion has a unique profile that suggests compensatory physiologic changes by
the left ventricle.
24. What is the pathophysiology of aortic stenosis?
Aortic stenosis is a fixed outlet obstruction to left ventricular ejection. Concentric hypertrophy (thick-
ened ventricular wall with normal chamber size) develops in response to the increased intraventricular
systolic pressure and increased wall tension necessary to maintain forward flow. Ventricular compliance decreases, and end-diastolic pressures increase. Contractility and ejection fraction are usually
maintained until late in the disease process. Atrial contraction may account for up to 40% of ventricular filling (normally 20%). Aortic stenosis is usually secondary to calcification of a congenital bicuspid
valve or rheumatic heart disease. Patients often present with angina, dyspnea, syncope, or sudden
death. Angina occurs in the absence of coronary artery disease because the thickened myocardium
is susceptible to ischemia (increased oxygen demand) and elevated end-diastolic pressure reduces
coronary perfusion pressure (decreased oxygen supply).
25. What is the pathophysiology of aortic insufficiency?
Chronic aortic insufficiency is usually rheumatic in origin. Acute aortic insufficiency may be secondary
to trauma, endocarditis, or dissection of a thoracic aortic aneurysm. The left ventricle experiences
volume overload, because part of the stroke volume regurgitates across the incompetent aortic
valve in diastole. Eccentric hypertrophy (dilated and thickened chamber) develops. A dilated orifice,
slower heart rate (relatively more time spent in diastole), and increased systemic vascular resistance increase the amount of regurgitant flow. Compliance and stroke volume may be significantly
increased in chronic aortic insufficiency, whereas contractility gradually diminishes. Ideally, such
patients should have valve replacement surgery before the onset of irreversible myocardial damage.
In acute aortic insufficiency, the left ventricle is subjected to rapid, massive volume overload with
elevated end-diastolic pressures and displays poor contractility. Hypotension and pulmonary edema
may necessitate emergent valvular replacement.
26. What is the pathophysiology of mitral stenosis?
Mitral stenosis is usually secondary to rheumatic disease. Critical stenosis of the valve occurs 10 to
20 years after the initial infection. As the orifice of the valve narrows, the left atrium experiences pressure overload. In contrast to other valvular lesions, the left ventricle shows relative volume underload
resulting from the obstruction of forward blood flow from the atrium. The elevated atrial pressure may
be transmitted to the pulmonary circuit and thus may lead to pulmonary hypertension and right-sided
heart failure. The overdistended atrium is susceptible to fibrillation with resultant loss of atrial systole,
leading to reduced ventricular filling and cardiac output. Symptoms (fatigue, dyspnea on exertion,
hemoptysis) may be worsened when increased cardiac output is needed, as with pregnancy, illness,
anemia, and exercise. Blood stasis in the left atrium is a risk for thrombus formation and systemic
embolization.
27. What is the pathophysiology of mitral regurgitation?
Chronic mitral regurgitation is usually due to rheumatic heart disease, ischemia, or mitral valve prolapse.
Acute mitral regurgitation may occur in the setting of myocardial ischemia and infarction with papillary
muscle dysfunction or chordae tendineae rupture. In chronic mitral regurgitation, the left ventricle and
atrium show volume overload, which leads to eccentric hypertrophy. Left ventricular systolic pressures
decrease as part of the stroke volume escapes through the incompetent valve into the left atrium, leading to elevated left atrial pressure, pulmonary hypertension, and eventually right-sided heart failure. As in
aortic insufficiency, regurgitant flow depends on valve orifice size, time available for regurgitant flow, and
transvalvular pressure gradient. The valve orifice increases in size as the left ventricle increases in size.
In acute mitral regurgitation, the pulmonary circuit and right side of the heart are subjected to sudden
increases in pressure and volume in the absence of compensatory ventricular dilatation, which may
precipitate acute pulmonary hypertension, pulmonary edema, and right-sided heart failure.
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